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Metabolism-regulating Non-coding RNAs in Breast Cancer: Roles, Mechanisms and Clinical Applications

Overview
Journal J Biomed Sci
Publisher Biomed Central
Specialty Biology
Date 2024 Feb 26
PMID 38408962
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Abstract

Breast cancer is one of the most common malignancies that pose a serious threat to women's health. Reprogramming of energy metabolism is a major feature of the malignant transformation of breast cancer. Compared to normal cells, tumor cells reprogram metabolic processes more efficiently, converting nutrient supplies into glucose, amino acid and lipid required for malignant proliferation and progression. Non-coding RNAs(ncRNAs) are a class of functional RNA molecules that are not translated into proteins but regulate the expression of target genes. NcRNAs have been demonstrated to be involved in various aspects of energy metabolism, including glycolysis, glutaminolysis, and fatty acid synthesis. This review focuses on the metabolic regulatory mechanisms and clinical applications of metabolism-regulating ncRNAs involved in breast cancer. We summarize the vital roles played by metabolism-regulating ncRNAs for endocrine therapy, targeted therapy, chemotherapy, immunotherapy, and radiotherapy resistance in breast cancer, as well as their potential as therapeutic targets and biomarkers. Difficulties and perspectives of current targeted metabolism and non-coding RNA therapeutic strategies are discussed.

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References
1.
Shelly M, Pinkas-Kramarski R, Guarino B, Waterman H, Wang L, Lyass L . Epiregulin is a potent pan-ErbB ligand that preferentially activates heterodimeric receptor complexes. J Biol Chem. 1998; 273(17):10496-505. DOI: 10.1074/jbc.273.17.10496. View

2.
Vander Heiden M, Cantley L, Thompson C . Understanding the Warburg effect: the metabolic requirements of cell proliferation. Science. 2009; 324(5930):1029-33. PMC: 2849637. DOI: 10.1126/science.1160809. View

3.
He M, Jin Q, Chen C, Liu Y, Ye X, Jiang Y . The miR-186-3p/EREG axis orchestrates tamoxifen resistance and aerobic glycolysis in breast cancer cells. Oncogene. 2019; 38(28):5551-5565. DOI: 10.1038/s41388-019-0817-3. View

4.
Schroeder B, Steen T, Espinoza I, Venkatapoorna C, Hu Z, Silva F . Fatty acid synthase (FASN) regulates the mitochondrial priming of cancer cells. Cell Death Dis. 2021; 12(11):977. PMC: 8531299. DOI: 10.1038/s41419-021-04262-x. View

5.
Guo D, Tong Y, Jiang X, Meng Y, Jiang H, Du L . Aerobic glycolysis promotes tumor immune evasion by hexokinase2-mediated phosphorylation of IκBα. Cell Metab. 2022; 34(9):1312-1324.e6. DOI: 10.1016/j.cmet.2022.08.002. View